Unveiling the virulence mechanism of Leptosphaeria maculans in the Brassica napus interaction: the key role of sirodesmin PL in the induction of cell death

Leptosphaeria maculans is the causal agent of blackleg disease in Brassica napus, leading to substantial yield losses. Sirodesmin PL, the principal toxin produced by L. maculans, has been implicated in the infection process in plants. However, the precise molecular and physiological mechanisms governing its effects remain elusive. This study investigates the changes induced by sirodesmin PL at the transcriptomic, physiological, and morphological levels in B. napus cotyledons. Sirodesmin PL treatment up-regulated genes associated with plant defense processes, including response to chitin, sulfur compound biosynthesis, toxin metabolism, oxidative stress response, and jasmonic acid/ethylene synthesis and signaling. Validation of these transcriptomic changes is evidenced by several typical defense response processes, such as the accumulation of reactive oxygen species (ROS) and callose deposition. Concomitantly, oxidized sirodesmin PL induced concentration- and exposure duration-dependent cell death. This cellular death is likely to be attributed to diminished activity of PSII and reduced number of chloroplasts per cell. In agreement, a down-regulation of genes associated with the photosynthesis process is observed following sirodesmin PL treatment. Thus, it is plausible that L. maculans exploits sirodesmin PL as a virulence factor to instigate cell death in B. napus during its necrotrophic stage, favoring the infection process. Sirodesmin PL, the principal toxin produced by Leptosphaeria maculans , induces cell death and defense mechanisms in Brassica napus , disrupting photosynthesis and facilitating the infection process.